Ebola, Chikungunya, Dengue and Zika have all been recently in the news. Many viruses, in particular RNA viruses, have short generation times and relatively high mutation rates (on the order of one point mutation or more per genome per round of replication for RNA viruses). This elevated mutation rate, when combined with natural selection, allows viruses to quickly adapt to changes in their host environment. The rapidity of viral evolution is problematic for the development of antiviral drugs, as resistant mutations often appear within weeks or months after the beginning of the treatment. One of the main theoretical models to study viral evolution is the quasispecies model, considering the virus as a quasispecies.1
It is important to remember that the rapid evolution of viruses is not one-sided. The host plays an important role, since the viruses use the cellular mechanisms of the host to replicate. Conceptualizing this interaction as a host-pathogen circuitry is a way to look at the complex relationship between viruses and hosts to better understand viral evolution. In this context, the interaction points and their origin are important to consider, such as viral single nucleotide varations, protein-protein interactions, post-translational modification of proteins, and host response data such as gene expression, genetic variations and even non-coding regions of host RNA.
In such a complex system, a major objective would be to identify key players in a network of dependencies and to select points of contact that could be influenced. This objective can only be achieved if the data that is generated is highly reliable and precise.
Next: Read about Precision Sequencing with CirSeq.
- Viral evolution. (2016, February 2).In Wikipedia, The Free Encyclopedia. Retrieved 19:50, February 16, 2016, from https://en.wikipedia.org/w/index.php?title=Viral_evolution&oldid=702928609 ↩